Obesity enhances the recruitment of mesenchymal stem cells to visceral adipose tissue

脂肪组织 骨髓 旁分泌信号 间充质干细胞 造血 脂肪生成 干细胞 肥胖 医学 脂肪因子 内科学 内分泌学 生物 化学 细胞生物学 瘦素 受体
作者
Agatha de Assis-Ferreira,Roberta Saldanha-Gama,Natália Mesquita de Brito,Mariana Renovato‐Martins,Rafael L. Simões,Christina Barja‐Fidalgo,Simone Vargas da Silva
出处
期刊:Journal of Molecular Endocrinology [Bioscientifica]
卷期号:67 (1): 15-26 被引量:9
标识
DOI:10.1530/jme-20-0229
摘要

In obesity, high levels of TNF-α in the bone marrow microenvironment induce the bone marrow-mesenchymal stem cells (BM-MSCs) towards a pro-adipogenic phenotype. Here, we investigated the effect of obesity on the migratory potential of BM-MSCs and their fate towards the adipose tissues. BM-MSCs were isolated from male C57Bl/06 mice with high-fat diet-induced obesity. The migratory potential of the BM-MSCs, their presence in the subcutaneous (SAT) and the visceral adipose tissues (VAT), and the possible mechanisms involved were investigated. Obesity did not affect MSC content in the bone marrow but increased the frequency of MSCs in blood, SAT, and VAT. In these animals, the SAT adipocytes presented a larger area, without any changes in adipokine production or the Sdf-1α gene expression. In contrast, in VAT, obesity increased leptin and IL-10 levels but did not modify the size of the adipocytes. The BM-MSCs from obese animals presented increased spontaneous migratory activity. Despite the augmented expression of Cxcr4, these cells exhibited decreased migratory response towards SDF-1α, compared to that of BM-MSCs from lean mice. The PI3K-AKT pathway activation seems to mediate the migration of BM-MSCs from lean mice, but not from obese mice. Additionally, we observed an increase in the spontaneous migration of BM-MSCs from lean mice when they were co-cultured with BM-HCs from obese animals, suggesting a paracrine effect. We concluded that obesity increased the migratory potential of the BM-MSCs and induced their accumulation in VAT, which may represent an adaptive mechanism in response to chronic nutrient overload.
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